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A cerebral hemorrhage or haemorrhage (or intracerebral hemorrhage, ICH) is a subtype of intracranial hemorrhage that occurs within the brain tissue itself. Intracerebral hemorrhage can be caused by brain trauma, or it can occur spontaneously in hemorrhagic stroke. Non-traumatic intracerebral hemorrhage is a spontaneous bleeding into the brain tissue.
A cerebral hemorrhage is an intra-axial hemorrhage; that is, it occurs within the brain tissue rather than outside of it. The other category of intracranial hemorrhage is extra-axial hemorrhage, such as epidural, subdural, and subarachnoid hematomas, which all occur within the skull but outside of the brain tissue. There are two main kinds of intra-axial hemorrhages: intraparenchymal hemorrhage and intraventricular hemorrhages. As with other types of hemorrhages within the skull, intraparenchymal bleeds are a serious medical emergency because they can increase intracranial pressure, which if left untreated can lead to coma and death. The mortality rate for intraparenchymal bleeds is over 40%.
Patients with intraparenchymal bleeds have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed. Other symptoms include those that indicate a rise in intracranial pressure due to a large mass putting pressure on the brain. Intracerebral hemorrhages are often misdiagnosed as subarachnoid hemorrhages due to the similarity in symptoms and signs. A severe headache followed by vomiting is one of the more common symptoms of intracerebral hemorrhage. Some patients may also go into a coma before the bleed is noticed..
Intracerebral bleeds are the second most common cause of stroke, accounting for 30–60% of hospital admissions for stroke. High blood pressure raises the risks of spontaneous intracerebral hemorrhage by two to six times. More common in adults than in children, intraparenchymal bleeds are usually due to penetrating head trauma, but can also be due to depressed skull fractures. Acceleration-deceleration trauma, rupture of an aneurysm or arteriovenous malformation (AVM), and bleeding within a tumor are additional causes. Amyloid angiopathy is a not uncommon cause of intracerebral hemorrhage in patients over the age of 55. A very small proportion is due to cerebral venous sinus thrombosis. Infection with the k serotype of Streptococcus mutans may also be a risk factor, due to its prevalence in stroke patients and production of collagen-binding protein.
Risk factors for ICH include:
Tramautic intracerebral Hematomas are divided into acute and delayed. Acute intracerebral Hematomas occur at the time of the injury while delayed intracerebral Hematomas have been reported from as early as 6 hours post injury to as long as several weeks. It is important to keep in mind that intracerebral Hematomas can be delayed because if symptoms begin to appear several weeks after the injury, concussion is no longer considered and the symptoms may not be connected to the injury.
Intraparenchymal hemorrhage can be recognized on CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain due to edema, and therefore shows up darker on the CT scan. Frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage or to detect a "spot sign".
Treatment depends substantially of the type of ICH. Rapid CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery.
The risk of death from an intraparenchymal bleed in traumatic brain injury is especially low when the injury occurs in the brain stem. Intraparenchymal bleeds within the medulla oblongata are almost always fatal, because they cause damage to cranial nerve X, the vagus nerve, which plays an important role in blood circulation and breathing. This kind of hemorrhage can also occur in the cortex or subcortical areas, usually in the frontal or temporal lobes when due to head injury, and sometimes in the cerebellum.
The inflammatory response triggered by stroke has been viewed as harmful in the early stage, focusing on blood-borne leukocytes, neutrophils and macrophages, and resident microglia and astrocytes. New area of interest are the Mast Cells.
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